Journals / Anadolu Kardiyoloji Dergisi / 2014 / Cilt: 14 - Sayı: 6

Assessment of serum hepcidin levels in patients with non-ST elevationmyocardial infarction

Pages
515–518
Publication Date
2022-10-10
DOI
—
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⚡ TL;DR(Too Long; Didn't Read)

However, serum troponin levels were increased significantly compared to baseline (0.29±3.56, 2.92±7.2 ng/mL, p

📌 3 Key Takeaways

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Objective & Hypothesis:Objective: Hepcidin is an acute-phase reactant produced in the liver displaying intrinsic antimicrobial activity.
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Key Findings & Data:We investigated in our study wheth-er the level of hepcidin has increased in the acute phase of non-ST elevation myocardial infarction patients (NSTEMI) known as acute inflam-matory aggravation of chronic atherosclerotic process.Methods: Seventy patients with NSTEMI and twenty healthy people were recruited as controls in this observational cross-sectional study.Serum hepcidin levels were determined by ELISA, and troponin levels were measured by standard laboratory methods.
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Conclusion & Impact:However, serum troponin levels were increased significantly compared to baseline (0.29±3.56, 2.92±7.2 ng/mL, p
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Abstract

Objective: Hepcidin is an acute-phase reactant produced in the liver displaying intrinsic antimicrobial activity. There are few studies abouthepcidin considered to be acute and chronic inflammatory marker in acute coronary syndromes patients. We investigated in our study wheth-er the level of hepcidin has increased in the acute phase of non-ST elevation myocardial infarction patients (NSTEMI) known as acute inflam-matory aggravation of chronic atherosclerotic process.Methods: Seventy patients with NSTEMI and twenty healthy people were recruited as controls in this observational cross-sectional study.Serum hepcidin levels were determined by ELISA, and troponin levels were measured by standard laboratory methods. Levels of hepcidin andtroponin were measured at admission and 6 hours later. Mean values of continuous variables were compared between groups using theStudent t-test or Mann-Whitney U test, according to whether normally distributed or not, as tested by the Kolmogorov-Smirnov test. Serumtroponin and hepcidin levels measured at admission and after 6th hours were compared using paired t-test.Results: Hepcidin level was similar between NSTEMI and controls at admission (24.55±32.13, 23.67±33.62 ng/mL, p>0.05, respectively). Also, serum hepcidinlevels did not change significantly from baseline in blood samples taken after 6 hour from admission in NSTEMI patients (24.55±32.13 ng/mL, 29.75±31.48ng/mL, p=0.62, respectively). However, serum troponin levels were increased significantly compared to baseline (0.29±3.56, 2.92±7.2 ng/mL, p

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Cite This Article

ALTUN, B., ALTUN, M., ACAR, G., KILINÇ, M., TAŞOLAR, H., KÜÇÜK, A., TEMİZ, A., GAZİ, E., KIRILMAZ, B. (2022). Assessment of serum hepcidin levels in patients with non-ST elevationmyocardial infarction. Anadolu Kardiyoloji Dergisi, Cilt: 14 - Sayı: 6, 515–518. https://ajindex.com/articles/436125

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References (1)

  1. Ross R. Atherosclerosis: an inflammatory disease. N Engl J Med 1999; 340: 115-26. [CrossRef] 2. Nemeth E, Valore EV, Territo M, Schiller G, Lichtenstein A, Ganz T. Hepcidin, a putative mediator of anemia of inflammation, is a type II acute-phase protein. Blood 2003; 101: 2461-3. [CrossRef] 3. Nicolas G, Chauvet C, Viatte L, Danan JL, Bigard X, Devaux I, et al. The gene encoding the iron regulatory peptide hepcidin is regulated by anemia, hypoxia, and inflammation. J Clin Invest 2002; 110: 1037-44. [CrossRef] 4. Nemeth E, Rivera S, Gabayan V, Keller C, Taudorf S, Pedersen BK, et al. IL-6 mediates hypoferremia of inflammation by inducing the synthesis of the iron regulatory hormone hepcidin. J Clin Invest 2004; 113: 1271-6. [CrossRef] 5. Suzuki H, Toba K, Kato K, Ozawa T, Tomosugi N, Higuchi M, et al. Serum hepcidin is elevated during the acute phase of myocardiyal infarction. Tohoku J Exp Med 2009; 218: 93-8. [CrossRef] 6. Isoda M, Hanawa H, Watanabe R, Yoshida T, Toba K, Yoshida K, et al. Expression of the peptide hormone hepcidin increases in cardiomyocytes under myocarditis and myocardial infarction. J Nutr Biochem 2010; 21: 749-56. [CrossRef] 7. Oğuz A, Uzunlulu M, Hekim N. Hepcidin is not a marker of chronic inflammation in atherosclerosis. Anadolu Kardiyol Derg 2006; 6: 239-42. 8. Hamm CW, Bassand JP, Agewall S, Bax J, Boersma E, Bueno H, et al. ESC Committee for Practice Guidelines. ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation: The Task Force for the management of acute coronary syndromes (ACS) in patients presenting without persistent ST-segment elevation of the European Society of Cardiology (ESC). Eur Heart J 2011; 32: 2999-3054. [CrossRef] 9. Simonis G, Mueller K, Schwarz P, Wiedemann S, Adler G, Strasser RH, et al. The iron-regulatory peptide hepcidin is upregulated in the ischemic and in the remote myocardium after myocardial infarction. Peptides 2010; 31: 1786-90. [CrossRef] 10. Hartford M, Wiklund O, Mattsson Hultén L, Perers E, Person A, Herlitz J, et al. CRP, interleukin-6, secretory phospholipase A2 group IIA, and intercellular adhesion molecule-1 during the early phase of acute coronary syndromes and long-term follow-up. Int J Cardiol 2006; 108: 55-62. [CrossRef]